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Remarkably, human immunodeficiency virus (HIV)-1 infects macrophages — immune cells that are equipped to detect pathogens and mediate innate immune responses — without stimulating innate immunity. Greg Towers and colleagues now show that this depends on the recruitment to the HIV-1 capsid of specific cofactors that are involved in orchestrating nuclear entry and targeting. When these capsid–cofactor interactions are prevented either by virus mutation, cofactor depletion or pharmacological inhibition of cofactor recruitment, viral DNA can be detected by innate immune sensors, including cyclic GMP-AMP synthase.